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PubMed2004

Improvement of graft prognosis in penetrating normal-risk keratoplasty by HLA class I and II matching.

BACKGROUND: Owing to contradictory results, HLA matching in penetrating keratoplasty still is equivocal. Different surgical techniques in multicentre studies, missing risk differentiation in high-risk situations, and faulty HLA typing can be identified as main reasons for these contradictory results. In this monocentre study, the value of HLA class I and II matching (A, B, DR loci) was examined in a homogeneous group of 418 normal-risk keratoplasty patients using serological typing techniques for HLA class I and immunogenetic typing techniques for class II. METHODS: Penetrating normal-risk keratoplasty was performed in two groups of patients (group I with 0-2, group II with 3-6 mismatches in the A/B/DR loci). All surgery was carried out by three experienced surgeons according to a standardized scheme. Furthermore, postoperative therapy and controls were standardized. There were no statistically significant differences between the two study groups with regard to the number of ABO or H-Y compatibilities, patient age, patient gender, ratio of previous intraocular surgery, ratio of triple procedures, indication for surgery, follow-up period, donor age, donor gender, post-mortem time of the graft, and endothelial cell density of the graft at the end of organ culture. All HLA typing was performed in a quality-controlled laboratory, serologically for HLA class I (A and B loci) and immunogenetically for HLA class II (DR locus). RESULTS: At 4 years postoperatively, the ratio of clear and rejection-free graft survival was 92% in group I and 66% in group II (Kaplan-Meier estimation, log rank test, P=0.03). Monovariate analysis in the Cox model gave no influence of solitary HLA class I or II matching, but only an influence of combined HLA class I and II matching (P=0.03). CONCLUSIONS: In this monocentre study with proper typing techniques, the beneficial effect of HLA class I plus II matching on clear and rejection-free graft survival could be demonstrated in a homogeneous group of normal-risk keratoplasty patients.

ABO Blood-Group System↗
PubMed1999

Nationwide collaborative study of HLA class II associations with distinct types of juvenile chronic arthritis (JCA) in Greece.

The aim of this study was to investigate the association of different groups and subgroups of juvenile chronic arthritis (JCA) with HLA class II (DR, DP, DQ) alleles and/or haplotypes. Groups and subgroups were mainly distinguished on the basis of the type of onset, the course and complications of the disease, and some predefined disease markers according to the criteria proposed by the ILAR Standing Committee (Chile, 1994). On the basis of these criteria the following five JCA groups and their subgroups were included in the study: (1) define systemic onset (n = 25) and systemic progressing to persistent arthritis (n = 14); (2) JCA of oligoarthritis onset (O-JCA, n = 124) and of oligoarthritis onset and course (n = 98), O-JCA of early (< 6 years) or late (> 6 years) onset (EOO-JCA n = 71 and LOO-JCA n = 44), O-JCA with ANA positive (n = 69) or negative (n = 55) and O-JCA progressing to extended arthritis (n = 22); (3) JCA of polyarthritis onset (P-JCA) with rheumatic factor (RF) negative (n = 29), and P-JCA RF negative with antinuclear antibodies (ANA) positive (n = 13) or negative (n = 16); (4) JCA complicated with chronic anterior uveitis (CAU, n = 32); (5) juvenile psoriatic arthritis (n = 20). To assess the HLA allele frequencies in the above 223 Greek children with JCA, these frequencies were compared to those of 98 age-matched and 250 adult controls. The main findings were the following. A common HLA-DRB1* allele was not involved in the JCA groups and subgroups studied; on the other hand, the DQA1*0501 allele was found to be associated with different JCA groups/subgroups (O-JCA, P-JCA RF-negative ANA-positive, JCA with CAU), probably suggesting a closer relationship of this locus with the immunogenetic background of JCA. The DPB1*0201 allele was associated with the development of either EOO-JCA or CAU. Susceptibility to CAU was stronger when the DPB1*0201 was combined with the presence of DRB1*13. Another allele, DQB1*0301, was also associated with O-JCA and CAU. Finally, no specific HLA class II allele was found to be related to the presence of ANA or psoriatic lesions or to the severity of the arthritis. Our findings suggest that the wide clinical and laboratory spectrum of JCA is associated with an immunogenetic background that is linked with HLA alleles of more than one locus. Some of them, such as the DPB1*0201 allele, confer susceptibility to certain clinical onsets and courses or complications of the disease. The rapidly advancing techniques of typing of DNA profiles may lead to more definite conclusions.

Adolescent↗
PubMed1995

Gene frequencies of the five major human platelet antigens in African American, white, and Korean populations.

BACKGROUND: The study of the immunogenetics of the human platelet antigens is important to the improvement of diagnosis and genetic counseling and to the development of screening programs for women at risk of having babies with neonatal alloimmune thrombocytopenia. Description of the immunogenetics of the human platelet antigens in some racial groups has been incomplete. STUDY DESIGN AND METHODS: A reverse dot blot technique employing polymerase chain reaction-amplified genomic DNA was applied in genotyping the five major human platelet antigens in the following populations: 100 African American and 100 white women admitted to the obstetric unit at Johns Hopkins Hospital (Baltimore, MD) and 100 inpatients at Yonsei University (Seoul, Korea). RESULTS: The gene frequencies of HPA-2b (Koa) and HPA-5b (Bra) in African Americans were twice those in whites (African Americans: 0.18 and 0.21, respectively; whites: 0.09 and 0.11, respectively). There is a very low gene frequency of the HPA-1b (PIA2) allele in Koreans (0.005). No significant differences were found in the gene frequencies of the human platelet antigens in whites in this series and those in published European studies. CONCLUSION: These studies indicate a higher potential risk for alloimmunization to HPA-2 (Ko) and HPA-5 (Br) antigens in African Americans than in whites. In addition, the low gene frequency of HPA-1b (PIA2) in African Americans and Koreans suggests that alloimmunization to HPA-1a (PIA1) would be very unusual in these populations. These data may provide the basis for planning neonatal alloimmune thrombocytopenia screening programs in certain ethnic populations.

Antigens, Human Platelet↗
PubMed2002

Experimental murine colitis is regulated by two genetic loci, including one on chromosome 11 that regulates IL-12 responses.

BACKGROUND & AIMS: Immunogenetic analysis of experimental colitis may contribute to the further unraveling of the complex genetic basis of the inflammatory bowel diseases, Crohn's disease and ulcerative colitis. METHODS: Genetic regions associated with susceptibility to trinitrobenzene sulfonic acid (TNBS)-induced colitis were identified in a genome-wide linkage analysis in F2 progeny of colitis-susceptible SJL/J and -resistant C57BL/6 mice. An immunogenetic approach was then used to further study the pathophysiologic role of one of the identified loci. RESULTS: We identified susceptibility loci on chromosomes 9 (Tnbs1) and 11 (Tnbs2). Tnbs2 harbors the interleukin (IL)-12 p40 gene, a likely candidate gene because IL-12 is a known central mediator for both experimental colitis and human Crohn's disease. We therefore tested the ability of colitis-susceptible and -resistant strains to mount IL-12 responses to lipopolysaccharide (LPS), a strong inducer of IL-12 that is abundantly present in the intestine. We observed a remarkably higher serum IL-12 response to LPS in susceptible SJL/J mice. Subsequently, we showed that the genetic region regulating the IL-12 response to LPS colocalizes with Tnbs2. CONCLUSIONS: These data strongly suggest that the tendency to mount a high LPS-induced IL-12 response and susceptibility to TNBS-induced colitis are related and that in fact a genetically determined high IL-12 response is involved in the immunologic basis of susceptibility to colitis.

Animals↗
PubMed2001

Role of cytokine gene polymorphisms in acute rejection and renal impairment after liver transplantation.

Although immunosuppressive regimens are effective, rejection occurs in up to 50% of patients after orthotopic liver transplantation (OLT), and there is concern about side effects from long-term therapy. Knowledge of clinical and immunogenetic variables may allow tailoring of immunosuppressive therapy to patients according to their potential risks. We studied the association between transforming growth factor-beta, interleukin-10, and tumor necrosis factor alpha (TNF-alpha) gene polymorphisms and graft rejection and renal impairment in 121 white liver transplant recipients. Clinical variables were collected retrospectively, and creatinine clearance was estimated using the formula of Cockcroft and Gault. Biallelic polymorphisms were detected using polymerase chain reaction-based methods. Thirty-seven of 121 patients (30.6%) developed at least 1 episode of rejection. Multivariate analysis showed that Child-Pugh score (P =.001), immune-mediated liver disease (P =.018), normal pre-OLT creatinine clearance (P =.037), and fewer HLA class 1 mismatches (P =.038) were independently associated with rejection. Renal impairment occurred in 80% of patients and was moderate or severe in 39%. Clinical variables independently associated with renal impairment were female sex (P =.001), pre-OLT renal dysfunction (P =.0001), and a diagnosis of viral hepatitis (P =.0008). There was a significant difference in the frequency of TNF-alpha-308 alleles among the primary liver diseases. After adjustment for potential confounders and a Bonferroni correction, the association between the TNF-alpha-308 polymorphism and graft rejection approached significance (P =.06). Recipient cytokine genotypes do not have a major independent role in graft rejection or renal impairment after OLT. Additional studies of immunogenetic factors require analysis of large numbers of patients with appropriate phenotypic information to avoid population stratification, which may lead to inappropriate conclusions.

Adult↗
PubMed2000

Genetic susceptibility and the link between cat exposure and rheumatoid arthritis.

OBJECTIVES: Rheumatoid arthritis (RA) is a chronic inflammatory disease for which immunogenetic susceptibility factors have been defined. In a recent case control study, it was shown that a prior intimate relationship with pet cats or budgerigars confers risk for subsequent development of RA after a period of latency. Pets are a potential reservoir for putative microbial agents that could be a stimulus for chronic inflammation subject to the influence of immunogenetic factors. Therefore, a study was undertaken to determine whether the presence of HLA-DRB1 alleles bearing the RA susceptibility motif influenced risk for RA associated with prior exposure to pets. METHODS: Blood samples were obtained from available RA patients and their case controls who had participated in the prior epidemiologic study. DR and DQ genotypes were determined by sequence analysis of oligonucleotides amplified from the DRB1 and DQB1 genes by polymerase chain reactions (PCR). Subjects were segregated according to pet exposure (as determined previously) and genotype for statistical analyses. RESULTS: The odds ratio (OR) for prepubertal exposure to cats and RA in available subjects irrespective of DRB1 genotype was 4.2 (CI, 2.1 to 8.5; P<.00002). The OR between prior exposure to cats and RA in subjects with the RA susceptibility genotype DRB1 *0401 and *0404 was 5.8 (CI, 1.4 to 26; P<.02) and >24 (CI, 1.6 to 813; P<.01), respectively. In subjects with the genotype DRB1 *1501, the association between RA and prior cat exposure was OR 8.4 (CI, 1.7 to 45; P<.01). No significant association between RA and pet exposure was found in patients selected according to other genotypes. The association between RA and the recognized HLA-DR susceptibility motif was slightly stronger in subjects with a history of intimate cat exposure (OR 4.7 [CI, 1.5 to 14.8], P<.005) than subjects without prior intimate exposure (OR 3.3 [CI; 1.2 to 9.3], P<.02). In the small number of subjects who had reported an intimate association with pet birds, no influence of DR genotype on risk for RA was discerned. CONCLUSIONS: Risk for RA associated with prior intimate exposure to cats is concentrated in subjects with the RA-susceptibility conferring genotypes DRB1 *0401 and *0404. The findings suggest an interaction between an environmen-tal agent associated with pet cats and certain RA susceptibility-conferring DR genotypes. The risk for RA associated with intimate cat exposure also was significant in subjects with DRB1*1501, a genotype not otherwise associated with RA, but which shares with known RA susceptibility-bearing alleles the presence of an electropositive pocket (Pocket 4) in the DR peptide binding groove.

Adult↗
PubMed1991

[T-lymphocyte subpopulation and HLA-DR antigens in hearing loss of vestibular neuropathy, Ménière's diseases and Bell's palsy].

In patients with various otoneurological diseases like hearing loss, neuronitis vestibularis, Ménière's disease and Bell's palsy, analyses concerning the immunoregulation and immunogenetics were done. For analysing the immunoregulation the T-helper (CD4) T-suppressor (CD8) ratio was determined. In contrast to patients with hearing loss caused by otobasal fractures and a healty control group, this ratio was elevated in 50% of the patients suffering from hearing loss. The elevation of the CD4/CD8 ratio was mainly caused by a reduction of CD8 positive cytotoxic-suppressor T-lymphocytes. The CD4/CD8 ratio may be of prognostic value, since an elevated ratio was found more often in patients with relapse of hearing loss, fluctuations, persistence of tinnitus or vestibular symptoms. An elevated ratio could also be detected in 48% of the patients with neuronitis vestibularis, in 50% of the patients with Ménière's disease and in 39% of the patients with Bell's palsy. A normal value was found in paralysis of the facial nerve of known origin like a state after trauma or after herpes zoster oticus paralysis. Immunogenetics was tested by HLA-DR typing. In patients with hearing loss HLA-DR4 antigen was distinctly increased, the relative risk was 2.8. The presence of the HLA-DR4 antigen proved to be an unfavourable sign, since in 44% of the patients presenting these antigens we found no improvement of the hearing. In patients with neuronitis vestibularis we found a relative risk of 3.12 and in patients with Ménière's disease a relative risk of 3.64, both for HLA-DR4.(ABSTRACT TRUNCATED AT 250 WORDS)

Facial Paralysis↗
PubMed2003

17. Immunologic endocrine disorders.

Immune-mediated tissue destruction or disregulation is the cause of multiple common, as well as rare, endocrine disorders including type 1 diabetes, Graves' disease, Hashimoto thyroiditis, and Addison's disease. Each of these disorders can be divided into a series of stages beginning with genetic susceptibility, environmental triggering events, and active autoimmunity, followed by metabolic abnormalities with overt disease. Common genetic susceptibility is suggested by the clustering of a series of disorders in the same individual and his or her family. A major portion of the genetic susceptibility lies in the HLA region, but for several disorders, mutation of transcription factors underlies disease susceptibility (eg, X-linked polyendocrinopathy, immune deficiency and diarrhea, and autoimmune polyendocrine syndrome type 1). With improving immunogenetic and pathogenic understanding, type 1A diabetes is now predictable, and excellent autoantibody screening assays are available. This knowledge, combined with studies in animal models, has led to trials for the prevention of diabetes. In addition, aberrant immunologic reactions (eg, insulin autoantibodies after insulin therapy, Graves' disease after monoclonal anti-T-cell therapy in multiple sclerosis) can complicate standard and experimental therapies. We therefore believe that an understanding of the immunogenetics and immunopathogenesis of endocrine disorders can aid in the prevention of morbidity and mortality for these related diseases.

Endocrine System Diseases↗
PubMed2000

Pemphigoid gestationis: a review.

Pemphigoid gestationis is a rare autoimmune vesiculobullous skin disease closely related to the pemphigoid group of blistering disorders. It is unique in that it is most frequently associated with pregnancy. Diagnosis is made on the basis of the presence of a subepidermal vesicle on routine histologic examination and of linear deposition of the third component of complement along the basement membrane zone of perilesional skin. Abnormal expression of major histocompatibility complex class II molecules in the placenta may trigger the initiating immunologic event in this organ, which is followed by cross-reactivity with an antigen present in the skin and the characteristic cutaneous signs of the disease. The immunogenetics of this disorder are interesting. A role for the involvement of major histocompatibility complex class II antigens seems likely because of the association with human leukocyte antigens DR3 and DR4. Major histocompatibility complex class III associations have also been observed, as has a high frequency of anti-human leukocyte antigen antibodies. We review the current understanding of the molecular biologic and immunogenetic properties of this disease and discuss treatment and potential impact on the fetus.

Diagnosis, Differential↗
PubMed1999

A 2-year prospective study in China provides epidemiological evidence for resistance in humans to re-infection with Schistosoma japonicum.

In 1996, 250 people living in the Dongting-Lake region of China were selected for a 2-year study. All had been or were infected with Schistosoma japonicum. All were treated with praziquantel, although eggs of S. japonicum were only detected in stool samples from 75 of the subjects. In 1998, 213 (85.5%) of these subjects, then with a mean (S.D.) age of 40.2 (14.2) years, provided stool samples for final assessment. Forty-nine (23%) of the 213 were found to be re-infected in 1998, with a geometric mean intensity of infection among the infected of 64.5 eggs/g faeces. The rate of re-infection was highest among those aged < 10 years, declining with increasing age, and higher in males than females (27.3% v. 8.3%; P < 0.005). The mean intensity of infection among the infected males was also higher than that among the infected females [72.4 (4.8) v. 17.8 (2.5) eggs/g; P < 0.005]. Water contact by the subjects was estimated from activity diaries, for 141 days over the 2-year study period, and expressed as skin exposure, in m2-min/day. The mean exposure of a group of subjects was calculated by detransforming the mean of the fourth-root-transformed (i.e. normalized) values for the exposures of each subject within the group. Overall, the 213 individuals had a mean exposure of 6.2 m2-min/day. Differences in occupation led to males having much higher mean water exposures than females (9.2 v. 1.1 m2-min/day). As there was an inverse association between age-specific exposure and age-specific re-infection intensity, the marked reduction seen in intensity of re-infection with increasing age is not attributable to decreasing exposure to water. Instead, the results of this 2-year cohort study provide evidence for age-dependent resistance to re-infection with S. japonicum. The 213 subjects who were followed up were classified, according to epidemiological outcome at the end of the study and the data on water contact, as 'susceptible' (N = 49; 23%), 'insusceptible' (N = 29; 13.6%) or of 'uncertain status' (N = 135; 63.4%). Thus, 78 subjects who are potentially informative in terms of immunogenetics were identified. Further investigation of these individuals should help to shed some light on the role of immunogenetic status in human immunity to Schistosoma japonicum.

Adolescent↗
PubMed1978

Disease associations of the Ia-like human alloantigens. Contrasting patterns in rheumatoid arthritis and systemic lupus erythematosus.

Increasing evidence has been obtained of the special value of Ia-like B-cell alloantisera for demonstrating disease associations with histocompatibility antigens. This was particularly evident for the study of the immunogenetics of rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), two conditions frequently considered related. The profiles of antigens recognized by the alloantisera in patients from each disease group was distinctive. Two types of alloantisera were obtained that illustrated the divergence between the twod iseases. One type showed a higher than normal incidence in RA but lower than normal in SLE; the other showed a higher incidence in SLE. While these sera were not totally defined, evidence was obtained that the SLE-reactive alloantiserum related to two alleles of the major histocompatibility complex DRw2 and DRw3, while the RA-reactive alloantiserum related to a common specificity shared by cells positive for either DRw4, DRw7, or DRw10. The data indicate that immunogenetic factors are relevant to the development of both RA and SLE, but that these are distinct for each disease.

Antigens, Surface↗
PubMed2003

Human leukocyte antigen class I and II alleles and response to interferon-alpha treatment, in Taiwanese patients with chronic hepatitis C virus infection.

To investigate the influence of immunogenetics on response to interferon (IFN)-alpha treatment, human leukocyte antigen alleles were characterized in 100 unrelated Taiwanese patients with chronic hepatitis C virus (HCV) infection. A11, B51, Cw15, and DRB1*15 were positively correlated with sustained response, whereas A24 was inversely associated with response to IFN-alpha, after adjustment for cirrhosis, pretreatment virus load, and viral genotype. Homozygote-genotype analysis showed that A24 and DQB1*05 probably had gene-dosage effect on sustained response. DRB1*15 was in strong linkage disequilibrium with DQB1*05 and DQB1*06, but only haplotype DRB1*15-DQB1*05 was associated with response to IFN-alpha. Haplotype A11-DRB1*15 was strongly associated with sustained response. This suggests a role for a complex host-immunogenetics interplay in the response to IFN-alpha, in patients with chronic HCV infection.

Adult↗
PubMed1999

MHC class II gene associations with autoantibodies to U1A and SmD1 proteins.

Autoantibodies against U small nuclear ribonucleoproteins (snRNP) are frequently present in the serum of patients with systemic rheumatic diseases, and have been reported to be associated with HLA-DR and -DQ genes. To better define the role of HLA genes in the production of such antibodies, we studied immunogenetic associations with autoantibodies reacting with U1 RNP, U1A and SmD1 proteins, and synthetic peptides containing immunodominant linear epitopes of these proteins. Only two out of the 15 overlapping peptides of U1A (i.e. peptides 35-58 and 257-282) and three of 11 peptides of SmD1 (i.e. peptides 1-20, 44-67 and 97-119) were significantly recognized by patients' sera selected on the basis of their antibody positivity with RNP in immunodiffusion. The distribution of DRB1, DQB1 and DPB1 alleles among the anti-RNP antibody-positive patients (n = 28) and healthy control subjects was similar. Antibodies against U1A (tested in Western immunoblotting with HeLa cell extracts) were positively associated to DRB1*06 allele; antibodies reacting with SmD1 peptide 44-67 were negatively associated to DRB1*02 and DQB1*0602 alleles. No association was found between DPB1 alleles and antibodies reacting with U1A and SmD1 antigens. This first study reporting an association between autoantibodies reacting with U1A and SmD1 proteins (and peptides of these proteins), and immunogenetic markers suggest that the production of antibody subsets directed against different components (or regions of these proteins) bound to the same snRNP particle is associated with distinct MHC class II alleles.

Alleles↗
PubMed1992

Association of DR3 with susceptibility to and severity of primary Sjögren's syndrome in a family study.

A study of HLA and primary Sjögren's syndrome (1 degree SS) was performed in 40 index cases and 180 relatives all of whom were Caucasian. The association of DR3 and 1 degree SS was confirmed. In probands, DR3 associated with extraglandular manifestations of 1 degree SS and homozygosity for DR3 associated with younger onset of disease. Familial clustering of 1 degree SS was evident. Definite or probable 1 degree SS (Fox criteria) occurred with a prevalence of 4.4% in the relatives, exclusively in older female first degree relatives and was associated with DR3. The relative risk was greatest in those who expressed anti-nuclear factor, rheumatoid factor or Ro and DR3. We identified a group of young females expressing some criteria for 1 degree SS and the same immunogenetic markers. They may be at risk of full expression of 1 degree SS as they become older. Milder forms of 1 degree SS were common in older relatives but not DR3 associated. 1 degree SS in males was rare and mild irrespective of immunogenetic status. Symptoms of 1 degree SS in relatives were mild or absent. Such individuals will only be identified through a family study or a community survey.

Adolescent↗
PubMed1980

Fetal pancreas allografts for reversal of diabetes in rats. I. Allograft survival in nonimmunosuppressed recipients.

Survival times of allogeneic fetal pancreases were determined across various immunogenetic barriers using several inbred rat strains. Pancreases from 17-day-old embryos transplanted beneath the kidney capsule of normal, nonimmunosuppressed recipients were richly vascularized within a short period regardless of histoincompatibilities. The transplants grew progressively, increased beta cell number, and synthesized insulin at a rate similar to that in isografts until rejection intervened. Survival end points were scored by (1) complete disappearance of intrinsic vascularization and necrotic change of tissue by gross observation of grafts, (2) a sharp decrease in insulin content in a graft as compared to that in a control isograft, and (3) destruction and disappearance of beta cells in histological examination. Although fetal pancreases were rejected within 10 days in all strain combinations, there were clear differences in host immune-reactions in terms of immunogenetic barriers between donor and recipient.

Animals↗
PubMed2000

The importance of H2 haplotype sharing in the induction of specific unresponsiveness by pretransplant blood transfusions.

BACKGROUND: The beneficial effect on graft survival achieved by pretransplant blood transfusions is well established. Previous studies have shown that the degree of major histocompatibility complex (MHC) (mis)-match between the transfusion donor and the recipient plays a determining role. However, other factors are also involved. In this study, we explored the hypothesis that, in addition to sharing of MHC antigens between the transfusion donor and the recipient, the MHC type of the organ donor is also of importance. METHODS: To mimic the human situation, F1 mice, rather than inbred strains, were pretreated with haplotype-shared allogeneic whole blood transfusions and transplanted with hearts of organ donors with different matched or mismatched H2 haplotypes. RESULTS: When a heart was transplanted 1 week after donor-specific transfusion (DST; blood transfusion donor=organ donor), an excellent prolongation of graft survival was obtained (median survival time: 77 days vs. 9 days in untreated mice). However, this was only the case when a haplotype was shared with the recipient; a DST given with no match between organ donor (=BT donor) and recipient did not induce any prolongation. Furthermore, in order to obtain the optimal beneficial effect of a haplotype-shared blood transfusion, the other haplotype of the transfusion donor had to be mismatched with the recipient. The immunogenetic studies showed that haplotype-shared blood transfusions in combinations where the H2 type of the organ donor differed from that of the transfusion donor are less efficient in inducing prolongation of graft survival. CONCLUSIONS: These results demonstrate that haplotype-shared blood transfusions can induce a significantly prolonged survival of cardiac allografts in F1 mice. The immunogenetic studies suggest that presentation of alloantigen-derived peptides in the context of self MHC (the indirect pathway of allorecognition) is essential for the beneficial effect of haplotype-shared blood transfusions.

Animals↗
PubMed1999

Contribution of major histocompatibility complex genes to susceptibility and resistance in Helicobacter pylori related diseases.

BACKGROUND/AIM: Although there have been numerous reports concerning the virulence factors of isolates for investigating the pathogenesis of Helicobacter pylori infection, few studies have been carried out regarding the association of HLA class II genes of the host with H. pylori related diseases. Two published studies have only analysed the HLA DQ locus alone. The aim of this study was thus to determine the association of HLA class II genes (DR, DQ and DP) with H. pylori related diseases using the DNA typing method. METHODS: Fifty-eight patients with H. pylori positive gastric ulcers, 44 patients with H. pylori positive duodenal ulcers, 45 patients with H. pylori positive gastritis and 34 healthy subjects without H. pylori infection were typed for HLA class II genes by means of DNA typing with the polymerase chain reaction-sequence specific oligonucleotide probes method. RESULTS: A negative association with DRB1*1501, DQA1*01021 and DQB1*0602 alleles was noted in all three of the patient groups studied. Compared with the healthy controls, a positive association with DPA1*0201 (P= 0.032) and DPB1*0901 (P=0.005) in gastric ulcers, a positive association with DRB1*0405 (P=0.022) and DQB1*0401 (P=0.044) in duodenal ulcers, and a positive association with DPB1*0901 (P=0.016) in gastritis were observed. A haplotype analysis showed that the association of alleles with H. pylori related disease was with the haplotype rather than with either of the alleles individually. After correction for multiple comparisons, all the significant associations obtained between H. pylori related diseases and HLA class II genes disappeared. CONCLUSIONS: The interplay between host immunogenetic factors, bacterial virulence factors and environmental conditions may thus play a more important role in the outcome of H. pylori infection than immunogenetic factors alone.

Adult↗
PubMed1997

Significantly increased occurrence of HLA-DQB1*0301 allele in patients with ocular cicatricial pemphigoid.

To determine the immunogenetic characteristics of patients with immune-mediated subepithelial blistering diseases of mucous membranes, we performed HLA-typing for the class II MHC gene DQB1*0301 allele using a direct method. Genomic DNA extracted from Caucasian patients was amplified by polymerase chain reaction using primer pairs specific for the DQB loci followed by Southern blotting with a peroxidase-conjugated sequence-specific oligonucleotide probe. Seventy-six percent (16/21) of patients with ocular mucosal disease (with or without oral mucosal and skin diseases) carried the DQB1*0301 allele; by contrast, only 33% (14/42) of race-, age-, and geography-matched normal individuals carried the DQB1*0301 allele (p < 0.005). The relative risk for ocular disease if DQB1*0301 allele is present is 6.4, similar to the relative risk of 8 for patients with ocular but no oral disease (pure ocular cicatricial pemphigoid, p < 0.025). In patients with oral mucosal disease (with or without ocular mucosal and skin diseases), 68% (15/22) carried the DQB1*0301 allele (p < 0.025). When patients with ocular disease were excluded, however, the increased occurrence of the DQB1*0301 allele in patients with oral disease was not statistically significant (64%, 7/11, p < 0.25). In patients with subepidermal blistering skin disease but no oral or ocular disease, there was no increase in the occurrence of the DQB1*0301 allele (38%, 5/13, p > 0.5). The significantly increased occurrence of the DQB1*0301 allele in patients with ocular mucosal disease may point to a distinct immunogenetic factor that predisposes patients to develop an ocular scarring process.

Alleles↗